We'll pay you later. So, I'll answer my version of that question as we're diving into this talk. So, the data around hypothermia and hemodynamic effects is actually conflicting. There's some data actually showing that despite the decrease in heart rate, the cardiac output actually goes up, and we know that global oxygen consumption goes down, so there might be a favorable hemodynamic effect, and there's also some animal data showing that there's a decrease in cardiac output. So, it's, at this point, I think, sort of a patient-by-patient decision, depending on how profoundly unstable they are. So, hello again, everybody. Nick Johnson from University of Washington. I'm gonna be talking about some of the other aspects of critical care management of the post-arrest patient, including some of the early diagnostics, mechanical ventilation, and then mechanical circulatory support. These are my disclosures. I have some research funding on cardiac arrests and other topics, and then I'm on a couple of scientific advisory boards and won't be talking about any of those specific devices today. So, overall, here are my goals for today. We're gonna talk about some of the advances in early diagnostics, including how we select patients to go to the cath lab for coronary angiography after cardiac arrest, and an emerging concept, which is the use of whole-body CT, like we use in trauma patients, but applied to the cardiac arrest patient. We'll talk about targets for oxygenation, ventilation, and hemodynamics, and then we'll talk about some of the emerging data around ECMO and other forms of mechanical circulatory support in the post-arrest or ongoing arrest patient. All right, but first, we'll do a little brain warmup. We'll have a couple multiple-choice questions embedded here. If you're feeling brave, feel free to raise your hand. Otherwise, just scribble it on a piece of paper or jot your answer down on your computer. All right, so based on the current evidence that we have, which patient is most likely to benefit from immediate coronary angiography? And I'll let you read the choices there, then we'll go through them. And I made these hard on purpose. All right, so who's voting for A? Anybody for A? All right, we've got a couple votes for A, great, great. How about B? All right, seems like that's the favorite so far. C? Couple votes for C. And D? All right, it seems like B is the winner, and you all are right, at least that's my version of the correct answer. And I think the reason this is the right answer is the cardiogenic shock component, and we'll talk a little bit more about why that is. So who needs urgent coronary angiography after cardiac arrest? There are a couple of cases where we know the answer, and these are patients with obvious ST elevation MI. And I say obvious because if you all have looked at a lot of post-arrest EKGs, you know that they can be wonky. We often see diffuse ST elevations, we might see ST elevations in non-anatomic distributions, sometimes we see wide or aberrant looking QRS complexes, and it's hard to sort out in the immediate post-arrest EKG what's true ischemia and what's global myocardial ischemia from global myocardial ischemia and reperfusion injury. So my current recommendation and strategy is to get a repeat ECG at least 10 minutes apart, and we'll talk about some recent studies on why that is. But if there's an obvious ST elevation MI in a consistent anatomic distribution, that's clear that patient should probably go to the cath lab just like any other patient with an obvious STEMI. There are some other patients that probably should also go. Patients who have electrical instability, so those who are going in and out of ventricular dysrhythmias, patients who have refractory cardiogenic shock, and then those in whom you have very high suspicion for ACS based on the clinical story. This might be a person where you get the history that they were running along a running trail in your hometown, they were complaining to their running partner of substernal crushing chest pain and then collapsed. In that patient, you have a high enough suspicion that this is likely ACS, there's a high pretest probability. I believe those patients should probably go for urgent coronary angiography as well. So the data on timing of ROSC to post-arrest EKG is really quite interesting. This is a study that came out of Italy from Enrico Baldi and their group, looking at the timing of ROSC and the post-arrest EKG and specificity for acute coronary ischemia. They found that patients that had very early ECGs perform within seven minutes of ROSC had a high likelihood of having a false positive for ACS. And as you go further out in time, the eight to 33-minute block, that false positive rate drops substantially and then there's diminishing returns after 30 minutes. So this has changed my practice in that now, I get my initial post-ROSC EKG, which for us is usually obtained in the pre-hospital setting for out-of-hospital arrest and get a repeat ECG at the 10-minute mark or so. So I know I'm in that sweet spot of a lower false positive rate, but I haven't lost time by waiting all the way out to that 33-minute window. So up until the past couple of years, we were really relying heavily on observational data around who should go to the cath lab after a cardiac arrest. And since 2019, we now have two randomized trials to help inform some of these decisions. The first that was published was the COACT trial published in the New England Journal in 2019. And this was a trial of about 600 patients with shockable initial rhythm and out-of-hospital cardiac arrest. The patients were randomized to a strategy of immediate coronary angiography or delayed, which they defined as delayed until after the neuroprognostication process was complete. What they actually got was a coronary angiogram within about two hours or within about five days. This trial importantly excluded two key patient populations. And this was the reason for answer B in the question that we started with. So patients with cardiogenic shock were excluded from this trial. So if patients had clear evidence of post-arrest cardiogenic shock, they were not included. Similarly, patients with electrical instability were excluded from this trial. Overall, the trial found no difference in the delayed versus immediate strategy with those important exclusions. And again, all of these patients did not have ST-elevation MI. Two years later, the Tomahawk trial was also published in the New England Journal. This trial also included about 550 patients. This trial, as opposed to COACT, included patients with all rhythms. And about half of the patients in this trial had an initial shockable rhythm. None of these patients had ST-elevation MI. They were excluded as well. And none of these patients had post-arrest cardiogenic shock. Trial had a similar strategy. They were randomized to immediate or delayed coronary angiography. And interestingly, in this trial, the immediate group actually did worse than the delayed group with a P-value that was 0.06, so not quite significant, but very close. The authors of this trial postulate a number of reasons why this group might have done worse. I think the reason that makes most sense to me is opportunity cost. If you're rushing patients off to the cath lab, what else are you not doing to stabilize those patients and look for other etiologies of their arrests, especially given that over half of this cohort was a non-shockable patient population, higher likelihood of having a non-coronary etiology for their arrest. So one of the other strategies that we've adopted at my institution, based on some of the data I'm about to tell you, is using, basically stealing, the trauma PAN scan from our trauma surgery colleagues and adapting it to cardiac arrest. We have a very dramatic name for this. We call it the CT sudden death, but you can call it whatever you want. My cardiology colleague, Kelly Branch, published our first experience with this, and there have been several papers that have been published on this topic since, and this was the experience with the first hundred patients or so. Our CT sudden death includes a non-contrast head CT. It also includes an ECG-gated chest CT that, in most cases, allows us to image the coronaries. There are some cases where, technically, that's not feasible. Usually, tachycardia is the limiting factor, but our chest radiologists are pretty amazing at reading these, even with heart rates in the normal range. And then that same chest CT also gives us the ability to look for pulmonary embolus or aortic pathology, as well as chest wall and other trauma related to CPR. We then scan through the abdomen and pelvis, mostly looking for complications in trauma related to CPR, which are pretty common in this population. So in the first 104 patients that we used this in, the etiology of the arrest was identified in 40% of patients, and this was not all comers. These were patients in whom the arrest etiology was not known, so it's an unselected patient population, but we found the etiology in almost half the patients. We also found a serious finding in 98% of patients. Most of these were CPR related injuries, which are, as you all know, exceedingly common. These were things like flail segments, multiple consecutive rib fractures that didn't quite meet flail criteria, pulmonary contusions, pulmonary lacerations, as well as some unusual things like a pericardial laceration, an intra-abdominal pathology, mostly solid organ injury related to lower rib fractures from CPR. So we think this is a relatively high yield test, especially given that most of these patients, or at least many of these patients, are gonna go on to additional therapies like the cath lab, or they're gonna get an angiogram, perhaps a stent, and dual antiplatelet therapy, and be at risk for bleeding complications. So identifying these injuries ahead of time can help us anticipate those things. All right, moving on to question number two. What is the best combination of blood pressure target and vasoactive agent in a post-arrest patient with mixed cardiogenic and distributive shock? All right, do we have any takers for A? Not seeing much love for A. B? C? All right, we've got some NOREPI aficionados in the crowd. And D? All right, great. The answer that I chose is C, and we'll talk a little bit about why. We'll talk a bit about blood pressure targets, and then I think Dr. Barlow is going to dive into agents a little bit more later, so we'll table that one for now. All right, so there's a pretty large body of observational data showing that higher mean arterial pressure is associated with better outcome after cardiac arrest. This is kind of intuitive. Patients who are not able to maintain a higher blood pressure do worse than patients who are able to maintain a higher blood pressure. But it turns out, a number of these studies actually adjust for the presence of vasoactives. And we now have a couple randomized trials, actually, on this specific topic. The best of these randomized trials was just published this year, called the BOX trial. And BOX is a two-by-two factorial design randomized trial that looked at both blood pressure and oxygenation targets, and they managed to nest a third randomized trial in there, looking at post-TTM temperature management, duration of temperature management. We're going to talk about the blood pressure arm now. So this trial included 789 comatose out-of-hospital arrest patients, two centers in northern Europe, and again, it was a two-by-two factorial design. The blood pressure arm randomized patients to a low or high mean arterial pressure target of 63 or 77. When I was first reading the abstract, I was like, why in the world would they choose those two numbers? They seem like odd blood pressure targets. But the design of this trial was actually really clever. This was a blinded trial. So they were able to blind clinicians to blood pressure. And the way they did this was they went to their clinical engineering department and they changed their blood pressure modules to have a fudge factor of 10% in either direction. So the clinicians were told, target a map of 70. What they actually were targeting was either a map of 63 or a map of 77, which is how they blinded the clinicians to what the blood pressure actually was. Quite clever, but that's the reason for the slightly odd map targets. The primary endpoint of this trial was death or hospital discharge with poor neurologic outcome defined according to the cerebral performance category score within 90 days. You can see down there in your bottom right panel that they got decent separation and met the blood pressure goals in the two different groups with some overlapping confidence intervals. And then in the Kaplan-Meier curve in the top, your left, there was no difference in the primary endpoint and there was no difference in any of their key secondary endpoints, including things like acute kidney injury and no difference in any adverse events with these two blood pressure targets. So the takeaway is with looking at all comers without a possible cardiac arrest, these two blood pressure targets, no difference between the groups. So reasonable to shoot for our typical map of 65 or a lower blood pressure target in most. Now, what this trial doesn't really address is what is the right blood pressure for the individual patient sitting in front of you based on their cerebral perfusion or some other index. We don't have a lot of great tools to measure this with high fidelity, which is something I think we're going to talk about a little bit later, but this is probably where we need to go. And I think one theme that you're hearing now in these first two talks is a lot of these trials look at population level interventions and what we probably need are patient physiology specific interventions. So just because higher blood pressure doesn't work in all comers, doesn't mean that there aren't some patients who might need this based on their individual auto-regulation status, their presence of existing cerebrovascular disease, or some other factor like their baseline blood pressure. But in all comers, a map of 65 seems to be a reasonable target. All right, moving on to my favorite topic in post-arrest care, oxygenation and ventilation, which of these values represents the best combination of PaO2 and PaCO2 for a comatose cardiac arrest patient who doesn't have severe cerebral edema on an initial head CT? And there are the choices, a lot of numbers, so I'll give you some more time for this one. Okay, any takers for A? We got one A in the back, a couple? All right, great. B? All right, lots of people like B. C? All right, we fear the hyperoxemia, I like it. And D? Okay, so it seems like B was the winner. That was the one I would choose as well. I'll try to justify that here in a second. So we've known for a long time that the way that we oxygenate and ventilate patients after cardiac arrest is linked with outcome. This was one of the earlier studies that was published all the way back in 2012 in JAMA by Hope Kilgannon. This study looked at over 6,000 post-arrest patients in the Project Impact database and found that patients who achieved hyperoxemia, which they defined as a PaO2 greater than 300, had higher mortality than patients who were maintained in the normal range. And both of those patients had a similar mortality to patients who were actually in the hypoxemic range with a PaO2 less than 60. So this was one of the earlier studies and earlier clinical studies showing that hyperoxemia was potentially associated with harm. There have been many of these since, mostly at large observational studies, but they all raise the same question, which is whether hyperoxemia is truly a biological problem, or are we creating oxygen-free radicals that are then being distributed throughout the body and injuring the brain and other organs, or is this just a marker for us paying less attention to the patient? If we're not turning down the FiO2, what else are we not doing? And it really wasn't until the past couple of years that we started to have some randomized trial data trickle out on this topic. Again, we're back to the box trial. This is the second factor of the box trial that was just published a few months ago. As a reminder, 789 comatose out-of-hospital cardiac arrest patients, two centers, and this is the oxygen factor. The oxygen arm was randomizing patients to two PaO2 ranges. The first was PaO2 of 68 to 75 millimeters of mercury, and then the liberal arm, it was 98 to 108 millimeters of mercury. So both in what I would consider relatively normal ranges of PaO2. Important to note that there were no patients that were randomized to PaO2s greater than 300. I think most of us probably in the modern era would not find that ethical to do. The primary outcome of this factor was the same, death or hospital discharge with poor neurological outcome. And again, they got pretty good separation in both PaO2 and FiO2, but there was no difference in their primary outcome, no difference in any of their key secondary outcomes, and no difference in any adverse events. So what this trial tells me is that we can maintain patients in a relatively normal range of PaO2 all the way from 60s to 100s. It does not tell me that it's safe to allow patients to be markedly hyperoxemic after cardiac arrest. We've not had that trial. I don't know that we ever will. So I still think that turning down the FiO2 is probably important, at least to get patients into a relatively normal range. Similar relationship or similar connection in observational data between PaCO2 and neurologic outcome. This is one of many observational studies showing an association between mild hypercarbia and favorable outcome after cardiac arrest. This was a study done in the Philadelphia region, a couple of different centers, where post-arrest patients had protocolized blood gases done at the one-hour mark and the six-hour mark. And they looked back to see what PaCO2 was most optimally associated with neurologic outcome. They found that in all comers, PaCO2 of 68 was most favorably associated with neurologic outcome. And then in the presence of concomitant metabolic acidosis, PaCO2 of 51 was most associated with favorable neurologic outcome. Again, difficult to know if this is biological effects or if this is just correlation. We do now have one phase two small randomized trial that was published on this topic of targeted mild hypercapnia. And why might this actually be a thing? Well, we know that CO2 is the most potent regulator of cerebral blood flow. And it might be that in the ischemic brain or the recently ischemic brain, mild therapeutic hypercarbia might promote cerebral vasodilation and improve perfusion. So this trial randomized patients to a PaCO2 of 35 to 45 or 50 to 55 for 24 hours after out of hospital cardiac arrest. And this was a pilot trial. So relatively small, about 40 patients. They got pretty good separation between the groups in terms of their PaCO2 targets. The primary endpoint for this trial was a biomarker, neuron-specific enolase, which is one of the biomarkers of neuronal injury. And they actually found that patients in the mild hypercapnia group compared to normocapnia had lower concentrations of this biomarker of neuronal injury, indicating that perhaps they had less brain injury. They also found a pretty whopping mortality difference favoring the mild hypercapnia group, but the trial wasn't powered to detect the mortality difference. But it did lead to this trial. So the TAME trial is an ongoing large phase three randomized trial of mild hypercapnia. This is based out of Australia and New Zealand. There have been 1,700 patients enrolled, which is their complete sample size. And they are now doing their analysis and waiting for all patients to meet their primary endpoint. Just like the phase two trial that they did, this trial randomized patients to PaCO2 of 50 to 55 versus 35 to 45 for 24 hours after cardiac arrest. The primary outcome is a neurological outcome at six months according to the Glasgow Outcome Scale. And from what I've heard, their last patient is nearing that six month point. So we should hopefully see results from this trial in the next several months. All right, so what about ARDS after cardiac arrest? This is a passion of mine. I think one of the things that we heard recently in the DeMar Hamlin case was a couple of days after he had his cardiac arrest, he was in the ICU at the University of Cincinnati and was being proned. And everyone was like, why would you prone a cardiac arrest patient? Well, this is why. We looked at about 600 cardiac arrest patients in our system who didn't die within the first 48 hours of after cardiac arrest. And about half of those patients actually went on to develop ARDS according to the Berlin's definition. And patients with ARDS compared with those who didn't have ARDS had more resource utilization in terms of ICU length of stay, ventilator days, and also had higher adjusted hospital mortality and a lower incidence of being discharged from the hospital neurologically intact. So we think this is one of the earlier papers to put ARDS on the map in terms of a post-cardiac arrest complication. Still has not been listed as an official etiology of ARDS, but we think it's an important one. And obviously these patients have a lot of other risk factors for ARDS that go along with their cardiac arrest, like chest wall trauma and aspiration being the big two. Similar story for in-hospital cardiac arrest. This is a study from a group in Boston just published this past year that also showed that a high proportion of in-hospital cardiac arrest patients, about 72% of the 200 patients they looked at met the Berlin definition for ARDS within 48 hours of their arrest. They also found an association between ARDS development and median alive and ventilator-free days over 28 days. So ARDS is common after both out-of-hospital and in-hospital cardiac arrest, and definitely is associated with more resource utilization and probably worse outcome. So can we do anything about it? Well, this is an observational study of low tidal volume ventilation after cardiac arrest. This does not just include patients with ARDS. This is all comers after out-of-hospital cardiac arrest. This was a study done at two centers, included about 250 patients, and they used propensity matching to compare patients who were ventilated with tidal volumes higher than eight milliliters per kilogram of predicted body weight with those who were ventilated with lower tidal volumes, less than eight mLs per kilo. Their predictor was time-weighted, predicted body weight-adjusted tidal volume in the first 48 hours. That is a mouthful. So they took tidal volume and they weighted it over time. And they found that tidal volumes less than eight mLs per kilo were associated with more favorable neurologic outcome, similar to our findings around ARDS. And lastly, in the respiratory bucket, this may be one of the only spaces where I've actually seen a signal for potential benefit for prophylactic antibiotics outside of perioperative antibiotics. This is not something I fully incorporated into clinical practice because it's such an outlier of a study and I'd like to see it replicated, but it is out there. So this is a placebo-controlled, double-blind randomized trial where patients after out-of-hospital cardiac arrest with shockable rhythm, interestingly, so these are not necessarily folks found down in a nursing home, were randomized to IV amoxiclov for 48 hours versus placebo, and their primary outcome was early-onset ventilator pneumonia, which they defined within seven days of the cardiac arrest event. And they actually found that the patients who got prophylactic antibiotics had a lower incidence of both early-onset VAP and also any VAP during their hospitalization. There was no difference in mortality and the trial wasn't powered for any of those outcomes. And there's a lot of criticisms around this outcome because as you all know, ventilator-associated pneumonia is in the eye of the beholder, even if you have relatively standardized definitions. Nonetheless, this is one of the few trials around VAP prevention that I've seen showing a benefit for systemic antibiotics to reduce the incidence of VAP. We do know from our imaging studies that we've done, the CT study that I showed you that now has about 600 patients enrolled, that the incidence of radiographic aspiration in these patients is basically 100%. Almost every patient has evidence of lung parenchymal abnormalities. So this may be a really high-risk population and this could be a real finding. But before I incorporate this into my practice for all comers, I'd like to see it replicated. All right, moving on to extracorporeal CPR. How many of you are working at centers where we're doing ECMO for ongoing cardiac arrest patients at this point? So a lot of you, yeah. So this is an area that I think is really exploding. And I think the arrest trial is part of that reason. A lot of you have probably read this by now, but this is Dimitri Yiannopoulos' arrest trial. This was a phase two open-label adaptive trial of patients with refractory ventricular fibrillation and cardiac arrest. And they defined refractory as patients who had persistent VF after three shocks. Patients had CPR initiated in the field and then were transported to the hospital and randomized where they either had their standard ACLS continued, standard resuscitation continued in the emergency department, or they were taken to the cath lab and emergently put on VA ECMO after which they had coronary angiography once they were hemodynamically stabilized. The take home from this trial is that it was stopped by their data safety monitoring board after 36 patients for overwhelming benefit. The ECPR group had six out of 14 patients survive, whereas the standard ACLS group just one out of 15. I think some of the more interesting work coming out of this really impressive group in Minneapolis who did the arrest trial is really around what the ICU course looks like for these patients. And I think as intensivists and other folks who work in the ICU, this is something that we should all be aware of if we're for institutions are diving into ECPR. These patients, I think probably consume more critical care resources than any other patient in the hospital. So this is an extremely resource intensive endeavor, not just in the beginning, but really for their whole hospital course. And you can see here, there's some striking things. So if you look at the red dots here, these are patients who start following commands. So our typical cardiac arrest patients, most of the patients who start waking up will do so within the first five days. These patients, some of them are waking up all the way out to day 15. So it really shows how long we need to continue to support these patients to accumulate additional neurologically intact survivors. Because in the past, patients who had 60 plus minutes of CPR, they weren't surviving. So we didn't really know what the course was. Now we know they have profound neurologic injury, but some of that recovers and it recovers all the way out to two weeks. Similar story for ICU utilization. These patients spend a long time in the unit. There are patients in the unit all the way out to the 30 day mark. And I know for those of us who are spending a lot of time taking care of patients with COVID ARDS on VVECMO, 30 days doesn't seem all that long, but for a cardiac ECPR patient, this is a long time in intensive care. So they've got some great descriptive stuff that they've written on sort of the ICU course and utilization and different complications these patients experience. And I think this highlights it well. What I've learned from our experience around ECPR is that it's not really just about being able to put cannulas in a patient. It's really building a system around this intervention that sets up for the potential of success. And that really begins in the pre-hospital setting with patient identification and selection, rapid transport to centers that are capable of performing this intervention. Getting the patient on is definitely an important piece of the story. And you really have to have folks who have expertise in cannulation and initiation. And then all the other components, including cardiovascular care and diagnostics, having interventional cardiologists willing to do coronary angiograms on people who are not really totally alive, but not quite dead either. And then the prolonged critical care and prolonged neurologic care that these patients require. And then something that we're gonna talk a little bit about in this session also is what recovery looks like for patients who've had an hour of cardiac arrest and all the related complications that go along with that. It's definitely prolonged and requires intensive rehab and a focus on survivorship. So building systems around this is probably the most important component to doing this successfully, not just getting a few folks interested who can put cannulas in. All right, what about other mechanical circulatory support devices? Well, there's some data around using the Impella, specifically the Impella CP during cardiac arrest. And this is the extent of the literature. Like 35 patients in a single registry, most of them had refractory VF and they were able to achieve a 30-day survival of 37%. But there's no comparison group, so we really have no idea what that's relative to. So there's really just not a lot of data around other forms of mechanical circulatory support, but I know there are centers out there experimenting with Impella and other devices during ongoing CPR to see if this might be a useful tool to increase the number of patients who survive. So where is this field headed? Well, I think this field is already headed into the field. There are a number of places that are experimenting in various ways with bringing this intervention to patients to try to really decrease the window between the arrest time and initiation of eCPR. The Minneapolis group already has their ECMO semi-truck, I would call it an ambulance, but it's not. There's an awesome photo out there on Twitter of Cindy sitting in the front of this thing. You could really get a sense of the scale, it's giant. But yeah, the Minneapolis group is now taking this portable cath lab to the patient and doing this procedure in the pre-hospital setting. They also have an ECMO copter, I believe, that is extending the reach of their group as well. And then there are a number of European groups, including this group in Paris. This is the famous picture of somebody getting put on eCPR in the Louvre, who have been taking eCPR to the patients for quite some time. And I think this is one approach to really decrease the window from the time of arrest to the time of ECMO initiation, which is probably key to success for eCPR at the systems level. So this is another really, really cool animal experiment that I think highlights a bit of the future for eCPR. This was a letter in the New England Journal that summarized a study that was actually published in Nature this year. This was an animal study where they anesthetized pigs and induced ventricular fibrillation. And then they let them have warm ischemia for a whole hour with no CPR. Then they attached them to this proprietary device that has a couple of key features, but they don't provide a ton of detail about what these are, because I'm guessing they either have or they're trying to patent this thing. But it's basically a VA ECMO circuit with a couple specific features. It has a pulse generator. So instead of the continuous flow that we typically see with VA ECMO, this is pulsatile blood flow. It also has a metabolic sensor. We don't know exactly what that means, but presumably it senses the electrolyte composition of the patient's reperfusate and titrates it in real time to some optimal formula. And it includes a hemodiafiltration. The pigs are bloodlet and they're reperfused with a hemoglobin-based oxygen carrier with a specific electrolyte composition. And what they found was quite remarkable. After an hour of warm ischemia, they were able to reestablish perfusion of all organs. These pigs were able to, when they were sacrificed eventually, they were able to determine that they had normal histologic structure in all of their organs, including the brain. They were able to restore all metabolic abnormalities. And they had some preliminary evidence that there was restoration of some neuronal function and that the pigs were spontaneously moving after this intervention. They compared to traditional VA ECMO and it was substantially better across the board than traditional VA ECMO. So this may be the future or some components of this may be the future. And it just goes to highlight that I think we're at the beginning of this extracorporeal circulation revolution. And we're really just figuring out how to do this. And I suspect the technology and the tools are gonna get rapidly better over the next few years. All right, so my take-homes, when we're caring for a post-arrest patient, really priority number one is to find out what happened and undo it so it doesn't happen again. I think a couple of the tools that we have are selective coronary angiography based on the factors we discussed. And I think there's growing literature to support that early CT should be a part of this as well. In terms of hemodynamics, I think when we're thinking about all comers MAP greater than 65 for most makes sense. And I think what we'll find in the coming years is it will be adjusting our mean arterial pressure and cerebral perfusion pressure goals to patient's specific targets. For oxygenation and ventilation, I still think turning down the FiO2 is important to avoid the extremes of hyperoxemia, but then maintaining patients in a normal range is probably reasonable. I keep the PaCO2 normal for now, but I'm keeping an eye out for that TAME trial, which could be published anytime, which might lead us toward permissive hypercarbia. We should remain vigilant for ARDS infection. And for those of you who are feeling like being on the cutting edge, mild permissive hypercapnia and prophylactic antibiotics might be for you. And then in terms of mechanical support and ECMO, all of these things require a really robust system to deploy. The recovery is prolonged and there are lots of ups and downs when you're caring for these patients. Patient selection is key. And I think we're gonna see a lot of evolution in the technology that will make this easier to do and improve outcomes over the next few years.

critical care management

post-arrest patients

hypothermia

hemodynamics

oxygen consumption

ECMO

mechanical circulatory support